Post Cardiac Arrest Care. From : 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Transcription

1 Post Cardiac Arrest Care From : 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

2 Initial Objectives of Post cardiac Arrest Care Optimize cardiopulmonary function and vital organ perfusion. After out-of-hospital cardiac arrest, transport patient to an appropriate hospital with a comprehensive post cardiac arrest treatment system of care that includes acute coronary interventions, neurological care, goal-directed critical care, and hypothermia. Transport the in-hospital post cardiac arrest patient to an appropriate critical-care unit capable of providing comprehensive post cardiac arrest care. Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest.

3 Subsequent Objectives of Post Cardiac Arrest care Control body temperature to optimize survival and neurological recovery Identify and treat acute coronary syndromes (ACS) Optimize mechanical ventilation to minimize lung injury Reduce the risk of multiorgan injury and support organ function if required Objectively assess prognosis for recovery Assist survivors with rehabilitation services when required

4 Systems of Care for Improving Post Cardiac Arrest Outcomes Most deaths occur during the first 24 hours after cardiac arrest. Multiple organ systems are affected, successful care will benefit from the development of system-wide plans Therapeutic hypothermia and treatment of the underlying cause of cardiac arrest impacts survival and neurological outcomes.

5 Systems of Care for Improving Post Cardiac Arrest Outcomes Proactive titration of hemodynamics to levels intended to ensure organ perfusion and oxygenation may improve outcomes. Programs should include therapeutic hypothermia; optimization of hemodynamics and gas exchange; immediate coronary reperfusion when indicated; glycemic control; and neurological diagnosis, management, and prognostication.

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7 Pulmonary System Pulmonary dysfunction after cardiac arrest is common. Etiologies: pulmonary edema from LV dysfunction; noncardiogenic edema from inflammatory, infective, or physical injuries; severe pulmonary atelectasis; or aspiration PEEP, a lung-protective strategy for mechanical ventilation, and titrated FIO2 are strategies that can improve pulmonary function and PaO2

8 Ventilation Rationale: Confirm secure airway and titrate ventilation Endotracheal tube when possible for comatose patients PETCO mm Hg Paco mm Hg

9 Chest X-ray Rationale: Confirm secure airway and detect causes or complications (eg, rib fracture, pneumothorax, and pleural effusions) of arrest: pneumonitis, pneumonia, pulmonary edema

10 Optimal FIO2 The optimal FIO2 during the immediate period after cardiac arrest is debated. The beneficial effect of high FIO2 on systemic oxygen delivery should be balanced with the deleterious effect of generating oxygen-derived free radicals during the reperfusion phase.

11 Pulse Oximetry/ABG Rationale: Maintain adequate oxygenation and minimize FIO2 SpO2 94% PaO2 100 mm Hg Reduce FIO2 as tolerated Pao2/FIO2 ratio to follow acute lung injury

12 Mechanical Ventilation Rationale: Minimize acute lung injury, potential oxygen toxicity Tidal Volume 6 8 ml/kg, inspiratory plateau pressure 30 cm H2O Titrate minute ventilation to PETCO mm Hg Paco mm Hg Reduce Fio2 as tolerated to keep Spo2 or Sao2 94% Low VT ventilation (6 ml/kg) increased incidence of atelectasis, PEEP may be warranted.

13 Avoid Hyperventilation Hyperventilation increases intrathoracic pressure ( Auto-PEEP) and inversely lowers cardiac output. The decrease in PaCO2 seen with hyperventilation can potentially decrease cerebral blood flow directly. Ventilation may be started at 10 to 12 breaths per minute and titrated to achieve a PETCO2 of 35 to 40 mm Hg or a PaCO2 of 40 to 45 mm Hg.

14 Frequent Blood Pressure Monitoring/Arterial-line Rationale: Maintain perfusion and prevent recurrent hypotension Mean arterial pressure 65 mm Hg or systolic blood pressure 90 mm Hg ScvO2 70%

15 Treat Hypotension Rationale: Maintain perfusion Fluid bolus if tolerated Dopamine 5 10 mcg/kg per min Norepinephrine mcg/kg per min Epinephrine mcg/kg per min

16 Continuous Cardiac Monitoring Rationale: Detect recurrent arrhythmia No prophylactic antiarrhythmics Treat arrhythmias as required Remove reversible causes

17 12-lead ECG/Troponin Rationale: Detect Acute Coronary Syndrome/ST-Elevation Myocardial Infarction; Assess QT interval

18 Treat Acute Coronary Syndrome Aspirin/heparin Transfer to acute coronary treatment center Consider emergent PCI or fibrinolysis. Concurrent PCI and hypothermia are safe and should not be deferred in the presence of coma or in conjunction with hypothermia.

19 Echocardiogram Rationale: Detect global stunning, wallmotion abnormalities, structural problems or cardiomyopathy, in order to guide ongoing management.

20 Use of Vasoactive Drugs After Cardiac Arrest Invasive monitoring: measure hemodynamic parameters accurately and determine the most appropriate combination of medications to optimize perfusion. Fluid administration as well as vasoactive (eg, norepinephrine), inotropic (eg, dobutamine), and inodilator (eg, milrinone) agents should be titrated as needed to optimize blood pressure, cardiac output, and systemic perfusion (Class I, LOE B).

21 Mechanical Circulatory Support Improves hemodynamics in patients not experiencing cardiac arrest It has not been associated with improved clinical outcome and routine use of mechanical circulatory support after cardiac arrest is not recommended.

22 Central Nervous System Brain injury is a common cause of morbidity and mortality in post cardiac arrest patients. Brain injury is the cause of death in 68% of patients after out-of-hospital cardiac arrest and in 23% after in-hospital cardiac arrest. Clinical manifestations include coma, seizures, myoclonus, various degrees of neurocognitive dysfunction (ranging from memory deficits to persistent vegetative state), and brain death.

23 Seizure Management Prolonged, untreated seizures are detrimental to the brain Common after ROSC, occurring in 5% to 20% of comatose cardiac arrest survivors with or without therapeutic hypothermia. EEG for the diagnosis of seizure should be performed with prompt interpretation as soon as possible and should be monitored frequently or continuously in comatose patients after ROSC (Class I, LOE C).

24 Seizure Management Neuroprotective agents with anticonvulsant properties such as thiopental and single-dose diazepam or magnesium have not improved neurological outcome in survivors. No studies: anticonvulsant therapy improves outcome, and several studies: post cardiac arrest seizures were refractory to traditional anticonvulsant agents. The same anticonvulsant regimens for the treatment of status epilepticus caused by other etiologies may be considered after cardiac arrest. (Class IIb, LOE C).

25 Prognostication of Neurological Outcome in Comatose Cardiac Arrest Survivors A thorough neurological evaluation is needed to obtain accurate prognostic findings. No postarrest physical examination finding or diagnostic study has as yet predicted poor outcome of comatose cardiac arrest survivors during the first 24 hours after ROSC.

26 Prognostication of Neurological Outcome in Comatose Cardiac Arrest Survivors After 24 hours SSEPs and select PE findings in the absence of confounders (such as hypotension, seizures, sedatives, or neuromuscular blockers) are the most reliable early predictors of poor outcome in patients not undergoing therapeutic hypothermia. The decision to limit care should never be made on the basis of a single prognostic parameter, and expert consultation may be needed.

27 Serial Neurological Exam Be reliably undertaken only in the absence of confounding factors (hypotension, seizures, sedatives, or neuromuscular blockers). Coma adult patients, not been treated with hypothermia, the absence of both pupillary light and corneal reflexes at 72 hours after cardiac arrest predicted poor outcome with high reliability.

28 Serial Neurological Exam The absence of vestibulo-ocular reflexes at 24 hours or GCS <5 at 72 hours are less reliable for predicting poor outcome or were studied only in limited numbers of patients. Other clinical signs, including myoclonus, are not recommended for predicting poor outcome (Class III, LOE C).

29 EEG An EEG pattern showing generalized suppression to <20 µv, burst-suppression pattern associated with generalized epileptic activity, or diffuse periodic complexes on a flat background: poor outcome No confounding factors such as sedatives, hypotension, hypothermia, neuromuscular blockade, seizures, or hypoxemia, an unprocessed EEG interpretation observed 24 hours after ROSC to assist with the prediction of a poor outcome in comatose survivors of cardiac arrest not treated with hypothermia (Class IIb, LOE B).

30 Evoked Potentials Bilateral absence of the N20 cortical response to median nerve stimulation after 24 hours predicts poor outcome in comatose cardiac arrest survivors not treated with therapeutic hypothermia (Class IIa, LOE A).

31 Consider Non-enhanced CT Scan Rationale: Exclude primary intracranial process

32 Blood and Cerebrospinal Fluid Biomarkers Unlikely to be confounded by sedation or neuromuscular blockade Neuron-specific enolase [NSE], predicting poor outcome when measured between 24 and 72 hours after cardiac arrest, disturbed by hypothermia, abdominal organ injury. The routine use of any serum or CSF biomarker as a sole predictor of poor outcome in comatose patients after cardiac arrest is not recommended (Class III, LOE B).

33 Changes in Prognostication With Hypothermia PE(motor response, pupillary light and corneal reflexes), EEG, SSEP, and imaging studies are less reliable for predicting poor outcome in patients treated with hypothermia. Durations of observation greater than 72 hours after ROSC should be considered before predicting poor outcome in patients treated with hypothermia (Class I, Level C).

34 Sedation/Muscle Relaxation Rationale: To control shivering, agitation, or ventilator desynchrony as needed

35 Sedation After Cardiac Arrest Opioids, anxiolytics, and sedativehypnotic agents can improve patientventilator interaction and blunt the stress-related surge of endogenous catecholamines. Neuromuscular blocking agents can be used for short intervals with adequate sedation.

36 Sedation After Cardiac Arrest Caution should be used in patients at high risk of seizures unless continuous EEG monitoring is available. Sedative agents should be administered cautiously with daily interruptions and titrated to the desired effect. Consider the titrated use of sedation and analgesia in critically ill patients who require mechanical ventilation or shivering suppression during induced hypothermia after cardiac arrest (Class IIb, LOE C).

37 Serial Lactate Rationale: Confirm adequate perfusion

38 Serum Potassium Rationale: Avoid hypokalemia which promotes arrhythmias Replace to maintain K >3.5 meq/l

39 Urine Output, Serum Creatinin Rationale: Detect acute kidney injury Maintain euvolemia Renal replacement therapy if indicated

40 Serum Glucose Rationale: Detect hyperglycemia and hypoglycemia Treat hypoglycemia (<80 mg/dl) with dextrose Treat hyperglycemia to target glucose mg/dl

41 Steroid No human randomized trials investigating corticosteroid use after ROSC The post cardiac arrest syndrome has similarities to septic shock, but the efficacy of corticosteroids remains controversial in patients with sepsis as well. The value of the routine use of corticosteroids for patients with ROSC following cardiac arrest is uncertain.

42 Avoid Hypotonic Fluids Rationale: May increase edema, including cerebral edema

43 Others Elevate the head of the bed 30 if tolerated to reduce the incidence of cerebral edema, aspiration, and ventilatory-associated pneumonia Attention should be directed to treating the precipitating cause of cardiac arrest after ROSC.

44 Brain injury and cardiovascular instability are the major determinants of survival after cardiac arrest. Because therapeutic hypothermia is the only intervention demonstrated to improve neurological recovery, it should be considered for any patient who is unable to follow verbal commands after ROSC.

45 Induced Hypothermia For protection of the brain and other organs, hypothermia is a helpful therapeutic approach in patients who remain comatose after ROSC. Randomized trials reported improved neurologically intact survival to hospital discharge when comatose patients with outof-hospital VF cardiac arrest were cooled to 32 C to 34 C for 12 or 24 hours beginning minutes to hours after ROSC.

46 Induced Hypothermia No randomized controlled trials have compared outcome between hypothermia and normothermia for non-vf arrest. Two nonrandomized studies with concurrent controls indicate a possible benefit of hypothermia after in- and out-of-hospital cardiac arrest associated with non-vf initial rhythms.

47 Induced Hypothermia Case series have reported the feasibility of using therapeutic hypothermia after ROSC in the setting of cardiogenic shock and therapeutic hypothermia in combination with emergent PCI. Case series report successful use of fibrinolytic therapy for AMI after ROSC, but data are lacking about interactions between fibrinolytics and hypothermia in this population.

48 When and Duration The impact of the timing of initiating hypothermia is not completely understood. Animal Models: short-duration hypothermia ( 1 hour) achieved <10 to 20 minutes after ROSC had a beneficial effect that was lost when it was delayed. Two trials: hypothermia was achieved within 2 hours or at a median of 8 hours had better outcomes in hypothermia-treated than normothermia-treated subjects Studies: time to target temperature (median 6.8 hours [IQR 4.5 to 9.2 hours]) was not an independent predictor of neurological outcome.

49 When and Duration The optimal duration of induced hypothermia is at least 12 hours and may be >24 hours. Hypothermia was maintained for 12 or 24 hours in the studies of out-of-hospital patients presenting in VF. The effect of a longer duration of cooling on outcome has not been studied in adults, but hypothermia for up to 72 hours was used safely in newborns.

50 Methods No single method has proved to be optimal. Endovascular catheters and surface cooling devices Iced isotonic fluid can be infused to initiate core cooling but must be combined with a follow-up method for maintenance of hypothermia.

51 Methods Case series: cooling can be initiated safely with IV ice-cold fluids (500 ml to 30 ml/kg of saline 0.9% or Ringer's lactate). Other series: Oxygenation was not significantly affected by the infusion of cold fluids (3427 ml 210 ml). Other trials: cooling with IV cold saline can be initiated safely in the prehospital setting.

52 Monitor Continuously monitor core temperature: esophageal thermometer, bladder catheter in nonanuric patients, or pulmonary artery catheter. Axillary and oral temperatures are inadequate for measurement of core temperature changes Tympanic temperature probes: rarely available and often unreliable. Bladder temperatures in anuric patients and rectal temperatures may differ from brain or core temperature.

53 Complication Coagulopathy, arrhythmias, and hyperglycemia, particularly with an unintended drop below target temperature. Pneumonia and sepsis may increase, prolonged hypothermia is known to decrease immune function. Hypothermia impairs coagulation, and any ongoing bleeding should be controlled before decreasing temperature.

54 Summary Comatose adult patients with ROSC after outof-hospital VF cardiac arrest should be cooled to 32 C to 34 C for 12 to 24 hours (Class I, LOE B). Induced hypothermia also may be considered for comatose adult patients with ROSC after in-hospital cardiac arrest of any initial rhythm or after out-of-hospital cardiac arrest with an initial rhythm of pulseless electric activity or asystole (Class IIb, LOE B).

55 Summary Active rewarming should be avoided in comatose patients who spontaneously develop a mild degree of hypothermia (>32 C) after resuscitation from cardiac arrest during the first 48 hours after ROSC. (Class III, LOE C).

56 Hyperthermia Temperature elevation above normal can impair brain recovery. No randomized controlled trials evaluating the effect of treating pyrexia Case series and studies: there is an association between poor survival outcomes and pyrexia 37.6 C.

57 Hyperthermia Patients can develop hyperthermia after rewarming posthypothermia treatment. This late hyperthermia should be identified and treated. Providers should closely monitor patient core temperature after ROSC and actively intervene to avoid hyperthermia (Class I, LOE C).

58 Core Temperature Measurement If Comatose Rationale: Minimize brain injury and improve outcome Prevent hyperpyrexia >37.7 C Induce therapeutic hypothermia if no contraindications Cold IV fluid bolus 30 ml/kg if no contraindication Surface or endovascular cooling for 32 C 34 Cx24 hours After 24 hours, slow rewarming 0.25 C/hr